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Article ; Online: Developmental estrogenization: Prostate gland reprogramming leads to increased disease risk with aging.

Prins, Gail S

Differentiation; research in biological diversity

2021 Volume 118, Page(s) 72–81

Abstract: While estrogens are involved in normal prostate morphogenesis and function, inappropriate early-life estrogenic exposures, either in type, dose or timing, can reprogram the prostate gland and lead to increased disease risk with aging. This process is ... ...

Abstract	While estrogens are involved in normal prostate morphogenesis and function, inappropriate early-life estrogenic exposures, either in type, dose or timing, can reprogram the prostate gland and lead to increased disease risk with aging. This process is referred to as estrogen imprinting or developmental estrogenization of the prostate gland. The present review discusses published and new evidence for prostatic developmental estrogenization that includes extensive research in rodent models combined with epidemiology findings that together have helped to uncover the architectural and molecular underpinnings that promote this phenotype. Complex interactions between steroid receptors, developmental morphoregulatory factors, epigenetic machinery and stem-progenitor cell targets coalesce to hard wire structural, cellular and epigenomic reorganization of the tissue which retains a life-long memory of early-life estrogens, ultimately predisposing the gland to prostatitis, hyperplasia and carcinogenesis with aging.
MeSH term(s)	Aging/genetics ; Aging/metabolism ; Aging/pathology ; Animals ; Animals, Newborn ; Carcinogenesis/genetics ; Epigenomics ; Estrogens/genetics ; Estrogens/metabolism ; Gene Expression Regulation, Developmental ; Genomic Imprinting ; Humans ; Hyperplasia/genetics ; Hyperplasia/metabolism ; Hyperplasia/pathology ; Male ; Prostate/metabolism ; Prostate/pathology ; Prostatitis/genetics ; Prostatitis/metabolism ; Prostatitis/pathology ; Receptors, Steroid/genetics ; Stem Cells/metabolism
Chemical Substances	Estrogens ; Receptors, Steroid
Language	English
Publishing date	2021-01-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	184540-8
ISSN	1432-0436 ; 0301-4681
ISSN (online)	1432-0436
ISSN	0301-4681
DOI	10.1016/j.diff.2020.12.001
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Article ; Online: Evaluating adverse effects of environmental agents in food: a brief critique of the US FDA's criteria.

Vandenberg, Laura N / Zoeller, R Thomas / Prins, Gail S / Trasande, Leonardo

Environmental health : a global access science source

2023 Volume 22, Issue 1, Page(s) 38

Abstract: Background: In the US, the Food and Drug Administration (US FDA) is charged with protecting the safety of food from both pathogens and chemicals used in food production and food packaging. To protect the public in a transparent manner, the FDA needs to ... ...

Abstract	Background: In the US, the Food and Drug Administration (US FDA) is charged with protecting the safety of food from both pathogens and chemicals used in food production and food packaging. To protect the public in a transparent manner, the FDA needs to have an operational definition of what it considers to be an "adverse effect" so that it can take action against harmful agents. The FDA has recently published two statements where, for the first time, it defines the characteristics of an adverse effect that it uses to interpret toxicity studies. Objective: In this brief review, we examine two recent actions by the FDA, a proposed rule regarding a color additive used in vegetarian burgers and a decision not to recall fish with high levels of scombrotoxin. We evaluated the FDA's description of the criteria used to determine which outcomes should be considered adverse. Overview: We describe three reasons why the FDA's criteria for "adverse effects" is not public health protective. These include an unscientific requirement for a monotonic dose response, which conflates hazard assessment and dose response assessment while also ignoring evidence for non-linear and non-monotonic effects for many environmental agents; a requirement that the effect be observed in both sexes, which fails to acknowledge the many sex- and gender-specific effects on physiology, disease incidence and severity, and anatomy; and a requirement that the effects are irreversible, which does not acknowledge the role of exposure timing or appreciate transgenerational effects that have been demonstrated for environmental chemicals. Conclusions: The FDA's criteria for identifying adverse effects are inadequate because they are not science-based. Addressing this is important, because the acknowledgement of adverse effects is central to regulatory decisions and the protection of public health.
MeSH term(s)	United States ; Food Safety ; United States Food and Drug Administration
Language	English
Publishing date	2023-04-21
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2092232-2
ISSN	1476-069X ; 1476-069X
ISSN (online)	1476-069X
ISSN	1476-069X
DOI	10.1186/s12940-023-00971-2
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Article ; Online: The Endocrine Society Centennial: Hormones and Apoptosis in the Prostate Gland… Live and Let Die.

Prins, Gail S

Endocrinology

2016 Volume 157, Issue 6, Page(s) 2197–2200

Language	English
Publishing date	2016-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2016-1192
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Article ; Online: Expression patterns of sex steroid receptors in developing mesonephros of the male mouse: three-dimensional analysis.

Omotehara, Takuya / Hess, Rex A / Nakata, Hiroki / Birch, Lynn A / Prins, Gail S / Itoh, Masahiro

Cell and tissue research

2023 Volume 393, Issue 3, Page(s) 577–593

Abstract: The androgen pathway via androgen receptor (AR) has received the most attention for development of male reproductive tracts. The estrogen pathway through estrogen receptor (ESR1) is also a major contributor to rete testis and efferent duct formation, but ...

Abstract	The androgen pathway via androgen receptor (AR) has received the most attention for development of male reproductive tracts. The estrogen pathway through estrogen receptor (ESR1) is also a major contributor to rete testis and efferent duct formation, but the role of progesterone via progesterone receptor (PGR) has largely been overlooked. Expression patterns of these receptors in the mesonephric tubules (MTs) and Wolffian duct (WD), which differentiate into the efferent ductules and epididymis, respectively, remain unclear because of the difficulty in distinguishing each region of the tracts. This study investigated AR, ESR1, and PGR expressions in the murine mesonephros using three-dimensional (3-D) reconstruction. The receptors were localized in serial paraffin sections of the mouse testis and mesonephros by immunohistochemistry on embryonic days (E) 12.5, 15.5, and 18.5. Specific regions of the developing MTs and WD were determined by 3-D reconstruction using Amira software. AR was found first in the specific portion of the MTs near the MT-rete junction at E12.5, and the epithelial expression showed increasing strength from cranial to the caudal regions. Epithelial expression of ESR1 was found in the cranial WD and MTs near the WD first at E15.5. PGR was weakly positive only in the MTs and cranial WD starting on E15.5. This 3-D analysis suggests that gonadal androgen acts first on the MTs near the MT-rete junction but that estrogen is the first to influence MTs near the WD, while potential PGR activity is delayed and limited to the epithelium.
MeSH term(s)	Male ; Animals ; Mice ; Mesonephros ; Androgens ; Epididymis ; Receptors, Estrogen ; Receptors, Androgen ; Gonadal Steroid Hormones ; Estrogens
Chemical Substances	Androgens ; Receptors, Estrogen ; Receptors, Androgen ; Gonadal Steroid Hormones ; Estrogens
Language	English
Publishing date	2023-06-19
Publishing country	Germany
Document type	Journal Article
ZDB-ID	125067-x
ISSN	1432-0878 ; 0302-766X
ISSN (online)	1432-0878
ISSN	0302-766X
DOI	10.1007/s00441-023-03796-0
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Article ; Online: Development priority.

Grandjean, Philippe / Prins, Gail S / Weihe, Pal

Basic & clinical pharmacology & toxicology

2019 Volume 125 Suppl 3, Page(s) 3–4

MeSH term(s)	Benzhydryl Compounds/adverse effects ; Congresses as Topic ; Embryonic Development/drug effects ; Endocrine Disruptors/adverse effects ; Environmental Exposure/adverse effects ; Environmental Pollutants/adverse effects ; Female ; Fetal Development/drug effects ; Humans ; Phenols/adverse effects ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced ; Prenatal Exposure Delayed Effects/prevention & control
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Environmental Pollutants ; Phenols ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2019-06-28
Publishing country	England
Document type	Editorial
ZDB-ID	2134679-3
ISSN	1742-7843 ; 1742-7835
ISSN (online)	1742-7843
ISSN	1742-7835
DOI	10.1111/bcpt.13249
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Article ; Online: Perfluorooctanesulfonic Acid Alters Pro-Cancer Phenotypes and Metabolic and Transcriptional Signatures in Testicular Germ Cell Tumors.

Boyd, Raya I / Shokry, Doha / Fazal, Zeeshan / Rennels, Brayden C / Freemantle, Sarah J / La Frano, Michael R / Prins, Gail S / Madak Erdogan, Zeynep / Irudayaraj, Joseph / Singh, Ratnakar / Spinella, Michael J

Toxics

2024 Volume 12, Issue 4

Abstract: The potential effects of poly- and perfluoroalkyl substances (PFAS) are a recently emergent human and environmental health concern. There is a consistent link between PFAS exposure and cancer, but the mechanisms are poorly understood. Although ... ...

Abstract	The potential effects of poly- and perfluoroalkyl substances (PFAS) are a recently emergent human and environmental health concern. There is a consistent link between PFAS exposure and cancer, but the mechanisms are poorly understood. Although epidemiological evidence supporting PFAS exposure and cancer in general is conflicting, there is relatively strong evidence linking PFAS and testicular germ cell tumors (TGCTs). However, no mechanistic studies have been performed to date concerning PFAS and TGCTs. In this report, the effects of the legacy PFAS perfluorooctanesulfonic acid (PFOS) and the newer "clean energy" PFAS lithium bis(trifluoromethylsulfonyl)imide (LiTFSi, called HQ-115), on the tumorigenicity of TGCTs in mice, TGCT cell survival, and metabolite production, as well as gene regulation were investigated. In vitro, the proliferation and survival of both chemo-sensitive and -resistant TGCT cells were minimally affected by a wide range of PFOS and HQ-115 concentrations. However, both chemicals promoted the growth of TGCT cells in mouse xenografts at doses consistent with human exposure but induced minimal acute toxicity, as assessed by total body, kidney, and testis weight. PFOS, but not HQ-115, increased liver weight. Transcriptomic alterations of PFOS-exposed normal mouse testes were dominated by cancer-related pathways and gene expression alterations associated with the H3K27me3 polycomb pathway and DNA methylation, epigenetic pathways that were previously showed to be critical for the survival of TGCT cells after cisplatin-based chemotherapy. Similar patterns of PFOS-mediated gene expression occurred in PFOS-exposed cells in vitro. Metabolomic studies revealed that PFOS also altered metabolites associated with steroid biosynthesis and fatty acid metabolism in TGCT cells, consistent with the proposed ability of PFAS to mimic fatty acid-based ligands controlling lipid metabolism and the proposed role of PFAS as endocrine disrupters. Our data, is the first cell and animal based study on PFAS in TGCTs, support a pro-tumorigenic effect of PFAS on TGCT biology and suggests epigenetic, metabolic, and endocrine disruption as potential mechanisms of action that are consistent with the non-mutagenic nature of the PFAS class.
Language	English
Publishing date	2024-03-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2733883-6
ISSN	2305-6304 ; 2305-6304
ISSN (online)	2305-6304
ISSN	2305-6304
DOI	10.3390/toxics12040232
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Article ; Online: Morphometric Analysis of Rat Prostate Development: Roles of MEK/ERK and Rho Signaling Pathways in Prostatic Morphogenesis.

Hu, Wen-Yang / Afradiasbagharani, Parivash / Lu, Ranli / Liu, Lifeng / Birch, Lynn A / Prins, Gail S

Biomolecules

2021 Volume 11, Issue 12

Abstract: The molecular mechanisms underlying prostate development can provide clues for prostate cancer research. It has been demonstrated that MEK/ERK signaling downstream of androgen-targeted FGF10 signaling directly induces prostatic branching during ... ...

Abstract	The molecular mechanisms underlying prostate development can provide clues for prostate cancer research. It has been demonstrated that MEK/ERK signaling downstream of androgen-targeted FGF10 signaling directly induces prostatic branching during development, while Rho/Rho-kinase can regulate prostate cell proliferation. MEK/ERK and Rho/Rho kinase regulate myosin light chain kinase (MLCK), and MLCK regulates myosin light chain phosphorylation (MLC-P), which is critical for cell fate, including cell proliferation, differentiation, and apoptosis. However, the roles and crosstalk of the MEK/ERK and Rho/Rho kinase signaling pathways in prostatic morphogenesis have not been examined. In the present study, we used numerical and image analysis to characterize lobe-specific rat prostatic branching during postnatal organ culture and investigated the roles of FGF10-MEK/ERK and Rho/Rho kinase signaling pathways in prostatic morphogenesis. Prostates exhibited distinctive lobe-specific growth and branching patterns in the ventral (VP) and lateral (LP) lobes, while exogenous FGF10 treatment shifted LP branching towards a VP branching pattern. Treatment with inhibitors of MEK1/2, Rho, Rho kinase, or MLCK significantly inhibited VP growth and blocked branching morphogenesis, further supporting critical roles for MEK/ERK and Rho/Rho kinase signaling pathways in prostatic growth and branching during development. We propose that MLCK-regulated MLC-P may be a central downstream target of both signaling pathways in regulating prostate morphogenesis.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Proliferation ; Fibroblast Growth Factor 10/metabolism ; Gene Expression Regulation, Developmental ; MAP Kinase Signaling System ; Male ; Morphogenesis ; Organ Culture Techniques ; Prostate/growth & development ; Prostate/metabolism ; Rats ; rho-Associated Kinases/metabolism
Chemical Substances	Fgf10 protein, rat ; Fibroblast Growth Factor 10 ; rho-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-12-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom11121829
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Article: Stem cells from a malignant rat prostate cell line generate prostate cancers

Hu, Wen-Yang / Liu, Li-Feng / Afradiasbagharani, Parivash / Lu, Ran-Li / Chen, Zhen-Long / Hu, Dan-Ping / Birch, Lynn A / Prins, Gail S

American journal of clinical and experimental urology

2022 Volume 10, Issue 6, Page(s) 377–389

Abstract: Cancer stem cells (CSCs) are resistant to conventional cancer therapies, permitting the repopulation of new tumor growth and driving disease progression. Models for testing prostate CSC-propagated tumor growth are presently limited yet necessary for ... ...

Abstract	Cancer stem cells (CSCs) are resistant to conventional cancer therapies, permitting the repopulation of new tumor growth and driving disease progression. Models for testing prostate CSC-propagated tumor growth are presently limited yet necessary for therapeutic advancement. Utilizing the congenic nontumorigenic NRP152 and tumorigenic NRP154 rat prostate epithelial cell lines, the present study investigated the self-renewal, differentiation, and regenerative abilities of prostate stem/progenitor cells and developed a CSC-based PCa model. NRP154 cells expressed reduced levels of tumor suppressor caveolin-1 and increased p-Src as compared to NRP152 cells. Gene knockdown of caveolin-1 in NRP152 cells upregulated p-Src, implicating their role as potential oncogenic mediators in NRP154 cells. A FACS-based Hoechst exclusion assay revealed a side population of stem-like cells (0.1%) in both NRP152 and NRP154 cell lines. Using a 3D Matrigel culture system, stem cells from both cell lines established prostaspheres at a 0.1% efficiency through asymmetric self-renewal and rapid proliferation of daughter progenitor cells. Spheres derived from both cell lines contained CD117
Language	English
Publishing date	2022-12-25
Publishing country	United States
Document type	Journal Article
ISSN	2330-1910
ISSN	2330-1910
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Article: Toward a Mechanistic Understanding of Poly- and Perfluoroalkylated Substances and Cancer.

Boyd, Raya I / Ahmad, Saeed / Singh, Ratnakar / Fazal, Zeeshan / Prins, Gail S / Madak Erdogan, Zeynep / Irudayaraj, Joseph / Spinella, Michael J

Cancers

2022 Volume 14, Issue 12

Abstract: Poly- and perfluoroalkylated substances (PFAS) are chemicals that persist and bioaccumulate in the environment and are found in nearly all human populations through several routes of exposure. Human occupational and community exposure to PFAS has been ... ...

Abstract	Poly- and perfluoroalkylated substances (PFAS) are chemicals that persist and bioaccumulate in the environment and are found in nearly all human populations through several routes of exposure. Human occupational and community exposure to PFAS has been associated with several cancers, including cancers of the kidney, testis, prostate, and liver. While evidence suggests that PFAS are not directly mutagenic, many diverse mechanisms of carcinogenicity have been proposed. In this mini-review, we organize these mechanisms into three major proposed pathways of PFAS action-metabolism, endocrine disruption, and epigenetic perturbation-and discuss how these distinct but interdependent pathways may explain many of the proposed pro-carcinogenic effects of the PFAS class of environmental contaminants. Notably, each of the pathways is predicted to be highly sensitive to the dose and window of exposure which may, in part, explain the variable epidemiologic and experimental evidence linking PFAS and cancer. We highlight testicular and prostate cancer as models to validate this concept.
Language	English
Publishing date	2022-06-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14122919
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Article ; Online: The Use and Misuse of Historical Controls in Regulatory Toxicology: Lessons from the CLARITY-BPA Study.

Vandenberg, Laura N / Prins, Gail S / Patisaul, Heather B / Zoeller, R Thomas

Endocrinology

2019 Volume 161, Issue 5

Abstract: For many endocrine-disrupting chemicals (EDCs) including Bisphenol A (BPA), animal studies show that environmentally relevant exposures cause harm; human studies are consistent with these findings. Yet, regulatory agencies charged with protecting public ... ...

Abstract	For many endocrine-disrupting chemicals (EDCs) including Bisphenol A (BPA), animal studies show that environmentally relevant exposures cause harm; human studies are consistent with these findings. Yet, regulatory agencies charged with protecting public health continue to conclude that human exposures to these EDCs pose no risk. One reason for the disconnect between the scientific consensus on EDCs in the endocrinology community and the failure to act in the regulatory community is the dependence of the latter on so-called "guideline studies" to evaluate hazards, and the inability to incorporate independent scientific studies in risk assessment. The Consortium Linking Academic and Regulatory Insights on Toxicity (CLARITY) study was intended to bridge this gap, combining a "guideline" study with independent hypothesis-driven studies designed to be more appropriate to evaluate EDCs. Here we examined an aspect of "guideline" studies, the use of so-called "historical controls," which are essentially control data borrowed from prior studies to aid in the interpretation of current findings. The US Food and Drug Administration authors used historical controls to question the plausibility of statistically significant BPA-related effects in the CLARITY study. We examined the use of historical controls on 5 outcomes in the CLARITY "guideline" study: mammary neoplasms, pituitary neoplasms, kidney nephropathy, prostate inflammation and adenomas, and body weight. Using US Food and Drug Administration-proposed historical control data, our evaluation revealed that endpoints used in "guideline" studies are not as reproducible as previously held. Combined with other data comparing the effects of ethinyl estradiol in 2 "guideline" studies including CLARITY-BPA, we conclude that near-exclusive reliance on "guideline" studies can result in scientifically invalid conclusions.
MeSH term(s)	Animals ; Benzhydryl Compounds/poisoning ; Benzhydryl Compounds/toxicity ; Ecotoxicology/methods ; Ecotoxicology/standards ; Endocrine Disruptors/poisoning ; Endocrine Disruptors/toxicity ; Environmental Exposure/adverse effects ; Environmental Exposure/analysis ; Guidelines as Topic ; Humans ; National Institute of Environmental Health Sciences (U.S.) ; Phenols/poisoning ; Phenols/toxicity ; Toxicity Tests/methods ; Toxicity Tests/standards ; United States ; United States Food and Drug Administration
Chemical Substances	Benzhydryl Compounds ; Endocrine Disruptors ; Phenols ; bisphenol A (MLT3645I99)
Language	English
Publishing date	2019-12-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqz014
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